Gastric Polyps: A Review on Clinical, Endoscopic, Histopathologic Features and Management Decisions

Rafiul Sameer Islam, MD, MBA, Neal C. Patel, MD, Dora Lam-Himlin, MD, and Cuong C. Nguyen, MD

Gastric Polyps: A Review on Clinical, Endoscopic, Histopathologic Features and Management Decisions

Rafiul Sameer Islam, MD, MBA, Neal C. Patel, MD, Dora Lam-Himlin, MD, and Cuong C. Nguyen, MD

Dr Islam and Dr Patel are gastroenterology fellows at the Mayo Clinic in Scottsdale, Arizona, where Dr Lam-Himlin is an assistant professor of laboratory medicine and pathology in the Department of Pathology and Dr Nguyen is an associate professor of medicine in the Division of Gastroenterology.

Address correspondence to: Dr Cuong C. Nguyen, Division of Gastroenterology, Mayo Clinic, 13400 East Shea Boulevard, Scottsdale, AZ 85259; Tel: 480-301-6990; Fax: 480-301-8673; Email:

Abstract: The increasing use of endoscopy has led to more discernable abnormalities in the stomach, including polyps. Gastric polyps encompass a spectrum of pathologic conditions that can vary in histology, neoplastic potential, and management. Despite their high prevalance, there is a paucity of literature to support managment and treatment decisions for endoscopists. The goal of this review is to summarize clinical, endoscopic and histopathologic features among various polyps, review syndromes associated with such polyps, and provide management recommendations.

With increasing use of endoscopy, visually discernible abnormalities, such as polyps in the gastrointestinal tract, are encountered more often. Gastric polyps most frequently originate in the mucosa, but encompass a broad spectrum of pathologic conditions that may be even submucosal or extrinsic. Found in 6% of upper endoscopies, gastric polyps are a heterogeneous group of epithelial and subepithelial lesions that can vary in histology, neoplastic potential, and management.1,2 Even though most are asymptomatic (>90%), larger polyps may present with bleeding, anemia, obstruction, or abdominal pain. Most have no risk of cancer, but there are certain subsets of polyps with malignant potential, necessitating further endoscopic treatment and/or periodic surveillance. These polyps are typically identified histologically since they have no reliable distinguishing endoscopic features. As many gastric polyps have similar endoscopic appearances, but their classification depends on the histologic compartments from which they arise; ie, epithelial, hamartomatous, or mesenchymal.

Epithelial Polyps

Epithelial polyps are the most commonly encountered gastric polyps. They include fundic gland polyps (FPG), hyperplastic polyps, and adenomatous polyps, all of which are associated with distinctly different clinical contexts, as discussed below. Other less common epithelial lesions that may present as polyps include neuroendocrine tumors (formerly “carcinoids”), ectopic pancreatic tissue, and pyloric gland adenomas.

Fundic Gland Polyps

FPSG are one of the most common polyps found in the stomach (47%),3 observed in 0.8% to 23% of all endoscopies.4-6 They come in 3 distinct clinical contexts: sporadic polyps, polyps associated with proton pump inhibitor use, and syndromic polyps (ie, familial adenomatous polyposis syndrome).

Sporadic FPG are sessile polyps located in the body and fundus.7 In general, their surface color is indistinguishable from that of normal gastric mucosa, and these lesions lack a stalk.8 On microscopy, they contain dilated glands lined by gastric body mucosa.4 Most endoscopists can diagnose these on appearance alone with 89% accuracy4; they appear as hyperemic, translucent, broad-based polyps with a smooth surface. Size varies from 1 mm to 8 mm and they are most commonly found in middle-aged women,9 although much larger polyps are also seen in adult men and women of all age groups.

These polyps are caused by an activating mutation of the beta-catenin gene, which is involved in cell growth signaling pathways.10-12 This subtype of FGP is not associated with atrophic gastritis, and the prevalence of Helicobacter pylori infection is low.13-16 In fact, H pylori seems to have a protective effect on FGP, since H pylori eradication is associated with polyp regeression.17 The risk of dysplasia in these polyps is diminutive, with a less than 1% chance of malignancy.18-20

Since 1993, there have been multiple reports of the role of proton pump inhibitors (PPIs)  in the development of gastric polyps.6,7 One particular study found FGPs in 23% of patients on PPIs, compared with a 12% incidence in patients not taking PPIs.6 Other large studies of patients who have been on long-term PPI therapy (defined as ≥5 years) had a 4-times higher prevalence for development of FGP.6,21 Furthermore, withdrawal of PPI therapy subsequently led to a reduction in FGPs. In addition to inducing enterochromaffin-like (ECL) cell hyperplasia, PPIs cause characteristic dilation of oxyntic glands and “parietal cell protrusions,” resulting in a histologically serrated glandular appearance.7,22

Familial Adenomatous Polyposis and Fundic Gland Polyps

Familial adenomatous polyposis (FAP) is an autosomal dominant disorder characterized by numerous epithelial-derived polyps located throughout the gastrointestinal tract, most commonly in the colon. This condition is caused by a germline mutation of the adenomatous polyposis coli (APC) tumor suppressor gene. The overall incidence of the mutation is between 1 in 10,000 and 1 in 15,000 births. By age 35 years, 95% of persons with FAP have polyps (>100 adenomas). The mean age of colon cancer in untreated persons is 39 years (range, 34–43 years).

Gastric polyps are reported in 30% to 100% of patients with FAP7; the large majority—95% —are fundic gland polyps (FGPs), while the remaining 5% are adenomatous polyps (discussed later). FGPs are exceptionally common in patients with FAP (20%–100%)23 and arise from a mutation in the APC gene.24 Unlike in the sporadic setting, FGPs associated with FAP usually carpet the body of the stomach. Dysplasia is seen in 25% to 41% of FAP associated FGPs,8 whereas it is rare in sporadic FGPs. It follows that when dysplasia is identified in a sporadic FGP, one should have a high index of suspicion for FAP syndrome.5,10,23 Unfortunately, there are no reliable endoscopic or histologic characteristics to distinguish FAP-associated polyps from sporadic FGPs. Clinical history and number of polyps are critical in this assessment, although the precise number of polyps needed to prompt further investigation is not defined.7 When present, dysplasia is typically low grade, and risk factors for dysplasia include large polyp size, higher Spigelman classification of duodenal polyposis, or the presence of antral gastritis.23

Current guidelines7 do not require polypectomy for sporadic FGP due to its low malignancy potential. However, despite the characteristic endoscopic appearance of FGP, biopsy is recommended at initial endoscopy to exclude dysplasia or adenocarcinoma and to exclude the need for further polypectomy if other types of polyps are present. FGPs  greater than1 cm should be resected due to sampling error from forceps biopsy alone.9 In patients with numerous polyps who are under the age of 40 years, especially in the absence of concurrent PPI use, or when biopsies demonstrate dysplasia, colonic investigation should be performed to exclude FAP, although the authors do admit to low evidentiary support for this recommendation.7 Surveillance endoscopy is not recommended for patients with nondysplastic sporadic FGPs.

Hyperplastic Polyps

The hyperplastic polyp is the second most common gastric polyp after the FGP. A common misnomer for them is inflammatory polyps, a term that should be discouraged because it can be confused with inflammatory fibroid polyps, which are managed much differently.7 Hyperplastic polyps are usually sessile or pedunculated, less than 2 cm in diameter,7 and typically occur in the antrum but can arise anywhere. Histologically, there is a proliferation of surface foveolar cells lining elongated, tortuous pits, imparting a corkscrew appearance that extends deep into the lamina propria. Gastric hyperplastic polyps may contain pyloric glands, chief cells, and parietal cells, and their histologic appearance can overlap with hamartomas and inflammatory conditions.7 The surface epithelium may also contain erosions or ulcerations leading to gastrointestinal bleeding.9

Unlike the incidental colonic hyperplastic polyp, gastric hyperplastic polyps do have clinical significance despite the similarities in nomenclature. Gastric hyperplastic polyps are strongly associated with inflammatory disorders such as chronic gastritis, H pylori gastritis, pernicious anemia, and reactive or chemical gastritis.11,25 As such, it is worthwhile to biopsy the background flat mucosa to identify any etiologic factors. In fact, when H pylori is the culprit, 80% of the hyperplastic polyps will regress with H pylori eradication, prior to endoscopic removal.26-28 Additionally, in areas adjacent to erosions/ulcer or gastroenterostomy sites, there can be multiple hyperplastic polyps.4,22

Interestingly, these polyps themselves have little neoplastic potential but are associated with an increased risk of synchronous cancer elsewhere in the gastric mucosa, particularly if associated with chronic gastritis.29 Unfortunately, the prevalence of dysplasia arising in hyperplastic polyps varies greatly, ranging from 1.9% to 19%, and cases of adenocarcinoma range from 0.6% to 2.1%.29-36 This discrepancy is most likely due to the small series of patients in the study populations, the location of the various studies (specifically in Asia), which tend to have a higher prevalence of gastric cancers in general, and the different sizes of hyperplastic polyps used as denominators in these studies.

Due to the low dysplastic potential of these polyps and the risk of synchronous cancers, it is not clear if hyperplastic polyps should be endoscopically resected or simply be biopsied. The lack of consensus stems from the concern that forceps biopsy sampling may miss the dysplastic foci within a hyperplastic polyp.7 The size cutoff for resection is debatable as well, with some authors recommending a 2-cm minimum for polypectomy,37 while others recommend resection of all polyps greater than 0.5 cm.30 Furthermore, the risk of adenocarcinoma in the surrounding nonpolypoid tissue is greater than in the polyp itself. As such, current recommendations require multiple biopsies of the flat uninvolved mucosa surrounding the polyp.7 Ultimately, it is the at endoscopist’s discretion to determine whether a polypectomy is warranted, relying on the size of the lesions and the clinical context. Testing for H pylori and eradication when present should be performed.7 Surveillance is recommended with a single repeat endoscopy at 1 year, but further surveillance subsequently is not recommended due to lack of evidence and should be an area for future research.7

Adenomatous Polyps

Gastric adenomas, or gastric polypoid dysplasia, are true neoplasms and are precursors to gastric cancer. Although commonly seen in countries with high gastric cancer rates (Korea, Japan, and China), they also account for 6% to 10% of all gastric polyps in Western populations.9 Histologically, they are classified similar to colon adenomas with tubular, villous, and tubulovillous distinctions. Frequently solitary, they are most commonly found in the antrum but can be located anywhere in the stomach. Endoscopically, they are often flat or sessile rather than pedunculated and can range in size from a few millimeters to centimeters9 (Figure 1). Atrophic gastritis and intestinal metaplasia are frequently associated with the development of these polyps, but there is no proven association with H pylori infection. Polyps that are greater than 2 cm and have villous histology have a higher risk of neoplasia (28%–40%).38-43 The presence of high-grade dysplasia is associated with an increased risk of invasive gastric cancer both within the polyp and in synchronous areas of the stomach.35,44

Due to the increased risk of malignancy associated with these polyps, recommendations include complete removal of the adenoma, with further examination of the entire gastric mucosa for abnormalities, all of which should be biopsied. Additionally, endoscopic follow-up is required following resection at 6 months (for incompletely resected polyps or high-grade dysplasia) or 1-year (for all other polyps). Operative resection should be considered for gastric adenomas that are not amenable to endoscopic resection. However, it should be noted that the most effective and optimal surveillance protocol for adenomatous polyps is yet to be established.

Gastric Neuroendocrine Tumors (Formerly Carcinoid)

Most gastric neuroendocrine tumors (NETs) are composed of ECL-like cells, typically in the corpus and fundus (90%),3 which stain with chromogranin A or synaptophysin by immunohistochemistry. There are 4 types of carcinoids in the stomach, each arising in different clinical contexts, and each with distinct prognoses and treatment protocols. This particular tumor underscores the importance of tandem biopsies of the background flat mucosa. Endoscopically, they appear as submucosal mass lesions, sometimes with ulcerations.45 In type I and II carcinoid, several polyps are seen in clusters arising nearly exclusively in the body fundic type mucosa. Type III lesions are usually solitary and may occur throughout the stomach. Type IV carcinoid may arise anywhere in the stomach and have a significantly worse prognosis. Histologically, these neuroendocrine tumors appear similar, and biopsies of the nonpolypoid mucosa are critical in distinguishing tumor type, prognosis, and treatment (Figure 2).

Type I neuroendocrine tumors are the most common. These occur in middle-aged women (70%–80%), and are the result of ECL cell hyperplasia arising in the setting of autoimmune metaplastic atrophic gastritis (AMAG, also known as autoimmune gastritis). The pathogenesis of type I neuroendocrine tumors is as follows: the autoimmune destruction of parietal cells leads to reduced gastric acid production and loss of feedback inhibition of gastrin secretion in the antral G cells. The resulting high levels of gastrin stimulate ECL cells to proliferate, which appear as multiple small nodules in the body of the stomach. Technically, this represents a reversible hyperplasia, but may progress to malignancy, especially as tumors enlarge.

Compared with type II and type III neuroendocrine tumors, type I lesions have an excellent prognosis with exceedingly low rates of metastatic disease.46 Endoscopic mucosal resection of any visible lesions and close endoscopic follow-up is prudent, but no existing guidelines or recommendations exist at this time and is an area of future research. Antrectomy to remove the stimulatory G cells has also proven useful as long-term therapy, and treatment of any underlying pernicious anemia is recommended.47 Biopsies of the background flat mucosa are critical in separating this low-risk tumor from others in the group.

Type II neuroendocrine tumors are rare and arise in the setting of multiple endocrine neoplasia 1 (MEN1) syndrome, Zollinger-Ellison syndrome, or a gastrin secreting tumor elsewhere in the gastrointestinal tract. The uninhibited gastrin secretion stimulates ECL cells to proliferate, resulting in gastric neuroendocrine tumors (often multiple). These type II tumors have worse prognosis than do type I, with metastasis in about 30% of cases.46 However, type II tumors behave distinctly better than type III tumors, again underscoring the importance of differentiating neuroendocrine tumor type, which can be achieved by providing tandem biopsies of the uninvolved background mucosa to the pathologist. Local resection of the neuroendocrine tumor, evaluation for metastatic disease, and resection of the stimulatory gastrin-secreting tumor (usually found in the small bowel) is the mainstay of therapy.46

Type III neuroendocrine tumor, the second most common type, has no associated clinical syndrome or context; rather, these lesions are sporadic. Whereas type I and type II tumors arise predominantly in the gastric body and are multiple, type III tumors can arise anywhere in the stomach and are typically solitary. In contrast to the excellent prognosis of type I and type II tumors, lymph node metastasis is found in 71% of type III tumors measuring more than 2 cm.48 In nearly all cases of type III tumors, surgical resection is advised.

Type IV neuroendocrine tumor , also known as poorly differentiated neuroendcrine carcinoma, are rare solitary tumors. They can arise in any part of the stomach and occur mainly in elderly men (>60 years). When diagnosed, these tumor are often large (50 – 70 mm) and ulcerated, and are believed to be a result of a primary defect of acid secretion by parietal cells. Unfortunately, at the time of diagnosis, most of these tumors are already in an advanced stage, with extensive metastasis, and are associated with a poor prognosis.49-51

Ectopic Pancreas

Ectopic pancreas is pancreatic tissue lacking anatomic and vascular continuity with the main body of the pancreatic gland.52,53 Located commonly in the stomach, they are small and are found incidently. Endoscopically, they appear to be a submucosal mass and can be misinterpreted for other submcosal tumors (ie, gastrointestinal stromal tumors  [GISTs] or leiomyomas).54 Central umbilication is frequently cited as the endoscopic clue to identify these lesions, although histologically proven ectopic pancreatic tissue can be seen without this endoscopic sign. These lesions have exceptionally low malignant potential.55,56

Pyloric Gland Adenomas

Pyloric gland adenomas are rare neoplasms that demonstrate gastric epithelial differentiation. They are composed of closely packed pyloric gland-type tubules with a monolayer of cuboidal to low columnar epithelial cells. They often arise in the gastric body with background mucosa showing features of autoimmune gastritis and intestinal metaplasia,57,58 and display a female predominance.59 These can often be mistaken for unusual gastric hyperplastic polyps; they are differentiated by displaying delicate ground glass cytoplasm without apical mucin.

Hamartomatous Polyps

Hamartomatous polyps are typically mucosal-based, but can be derived from any of the 3 embryonic layers. These polyps result from disordered growth of tissues indigenous to the site. Examples include Peutz-Jeghers polyps and juvenile polyps, as well as hamartomatous polyps without specific names. These can be either sporadic in nature, or are associated with various polyposis syndromes such as Peutz-Jeghers syndrome, juvenile polyposis syndrome, and Cowden syndrome (PTEN or multiple hamartoma syndrome), as discussed below.

Peutz-Jeghers Polyps and Syndrome

Peutz-Jeghers syndrome is an autosomal dominant hereditary disorder with a unique constellation of findings, including hamartomatous polyps throughout the gastrointestinal tract and mucocutaneous hyperpigmentation, most notably of the lips.60 Although patients with this syndrome are more likely to have small bowel or colonic polyps, gastric polyps occur in about 15% to 30% of patients.61 Peutz-Jeghers polyps have a characteristic glandular epithelium with dilated cystic glands, which are supported by an arborizing framework of well-developed smooth muscle that is contiguous with the muscularis mucosa. In the small bowel and colon, these lesions can be differentiated from juvenile polyps, as Peutz-Jeghers polyps have intact lamina propria with a “fanning out” appearance of the smooth muscle fibers (Figure 3). However, gastric syndromic polyps are often indistinguishable from nonspecific gastric hyperplastic polyps.62 Consequently, it is imperative that the interpreting pathologist be provided with complete endoscopic and clinical information to ensure a proper diagnosis. Furthermore, it should be pointed out that when a hamartomatous syndrome is suspected, polyps from the small bowel and colon are more likely to be diagnostic.

Peutz-Jeghers polyps have malignant potential and the average age of patients presenting with gastric carcinoma is estimated to be 30 years.61 Current recommendations suggest screening for gastric polyps as early as ages 8 to 21 years. Gastric Peutz-Jeghers polyps larger than 1 cm should be resected endoscopically, and patients should receive annual surveillance.7 For patients with smaller (<1 cm) polyps, surveillance endoscopy every 2 to 3 years is recommended,60 although it is recognized that, in certain clinical settings, small polyps can be removed.

Juvenile Polyps and Juvenile Polyposis Syndrome

Juvenile polyps (JPs) are mucosal tumors that consist primarily of an excess of lamina propria and dilated cystic glands; therefore, they are classified as hamartomatous polyps (Figure 4). Occasionally they are referred to as “inflammatory” or “retention polyps” due to the appearance of distended, mucus-filled glands, inflammatory cells, and edema. JPs are typically solitary pedunculated lesions in the antrum and range from 3 mm to 20 mm. When found alone, they are believed to be benign incidental lesions, unassociated with a syndrome. However, when multiple JPs are seen, a syndrome of juvenile polyposis should be considered. Since this is a clinical-pathologic diagnosis, the communication of a complete profile of endoscopic and clinical information is a sine qua non for the pathologist’s success. Juvenile polyposis is an autosomal dominant disorder that carries a lifetime gastric malignancy risk of greater than 50%.63 Thus, for juvenile polyposis syndrome, endoscopic screening is recommended beginning at age 18 years and every 3 years thereafter. 7

Cowden Syndrome

Cowden syndrome is another autosomal dominant, multisystem disorder characterized by hamartomatous tissue overgrowth of all 3 embryonic layers (Figure 5). Eighty percent of patients have a germline mutation of the PTEN tumor suppressor gene.64 There are several pathognomonic criteria for the diagnosis of this syndrome, including facial trichilemmomas, acral keratoses, and papillomatous papules. Once again, just like other clinical-pathologic diagnoses, the importance of full communication between the endoscopist and the pathologist cannot be over-emphasized. Cowden syndrome has a slight female preponderance, and the age of diagnosis ranges from 16 to 65 years. Transformation of gastrointestinal polyps to malignancy is thought to be extremely rare, thus surveillance endoscopy has not been recommended by most. However, disorders and malignancy of the breast, thyroid, and genitourinary tract are more common and, thus, further clinical investigation is warranted when this diagnosis is suggested on endoscopic biopsy.

Mesenchymal Polyps

Mesenchymal lesions cover a broad spectrum of mesodermally derived tumors. These polyps can be mucosal or submucosal in location, but are typically situated underneath the surface epithelium, imparting a more nodular than polypoid appearance. Given their deep location, these lesions should be further evaluated by endoscopic ultrasound and tissue acquisition. Select common mesenchymal polyps covered herein include inflammatory fibroid polyps, GISTs, leiomyomas, and granular cell tumors.

Inflammatory Fibroid Polyps

Inflammatory fibroid polyps (IFPs), or Vanek polyps/tumors, usually present as  polypoid lesions or nodules. These histologically unique lesions, arising in the submucosa, were first described in 1949 by Vanek under the name “gastric submucosal granulomas with eosinophilic infiltration.”65 These lesions are characterized by CD34 immunoreactive spindle and stellate stromal cells mixed with inflammatory cells (predominantly eosinophils) and edema (Figure 6). Although once believed to be a reactive lesion, recent studies have proven that this lesion is neoplastic by identifying activating mutations in the platelet-derived growth factor receptor alpha (PDGFRα). This mutation is also found in a subset of gastrointestinal stromal tumors, typically the gastric benign epithelioid variant that do not have a CD117 (proto-oncogene cKit) mutation. IFPs are now viewed as PDGFRα-driven benign neoplasms.66

These polyps also contain myxoid stroma and often thin-walled vessels. IFPs can occur in all ages but are most common at 50 to 60 years and have a slightly higher incidence in women.3 They are rare lesions with an estimated relative prevalence of 0.09%.1,67

IFPs present most often as solitary lesions in the gastric pylorus or distal antrum and are typically small (<1.5 cm) and sessile.66 They rarely cause clinical symptoms; however a few cases of large gastric IFPs causing gastric outlet obstruction have been reported.68 They are believed to have no malignant potential; thus, no endoscopic follow up is recommended after initial histologic confirmation. Larger and/or symptomatic lesions may require complete endoscopic resection by an experienced endoscopist.13

Gastrointestinal Stromal Tumors

GISTs are rare connective tissue tumors originating in the muscularis propria, and account for 1% to 3% of all malignant gastrointestinal tumors.69 Newer estimates show up to 5000 new cases per year in the United States.70,71 These tumors are often found incidentally during upper endoscopy performed for reasons or symptoms unrelated to the tumor.72 The clinical features can vary depending on the anatomic location, size, and aggressiveness of the tumor. Although these tumors may arise anywhere along the luminal gastrointestinal tract, the most common site is the stomach. These lesions are derived from the interstitial cells of Cajal (the pacemaker cells of the gastrointestinal tract), which reside between the inner circular and outer longitudinal layers of the muscularis propria. GISTs have a mutation of the proto-oncogenes KIT or PDGFRA with known positivity for CD117 in 95% of the tumors.7 Although most GIST (>90%) exhibit cytoplasmic immunoreactivity for CD117, a proportion can be CD117-negative. These particular GISTs will stain with DOG-1 immunohistochemistry, an equally sensitve and specific GIST marker.71,73,74 Additionally, a subset of lesions, particularly in the context of Carney and Stratakis syndrome, may have a mutation of the succinate-dehydrogranse gene.75 The most reliable prognostic factors for GISTs are site and size of the primary tumor and mitotic index. Endoscopic ultrasound and computed tomography scan are important to determine local and metastatic spread.76-78

Treatment is dependent on the stage of the tumor. If localized to the stomach, it can be surgically resected. If the tumor is metasatic or unresectable, imatinib  is the first-line chemotherapeutic agent of choice in tumors expressing c-Kit mutation (Figure 7). Additionally, genotyping GISTs has become an important therapeutic intervention for stratifying treatment options with neoadjuvant or adjuvant imatinib.79-81 Although patients with large (>2 cm) or symptomatic GISTs will need surgical interventions, many other patients may not. Unfortunately, there have been no large prospective studies to evaluate the use of routine endoscopic ultrasound (EUS) surveillance strategies.82 Nonetheless, case reports of adequate endoscopic resection of small GISTs using various techniques exist.83-89


Leiomyomas are benign smooth muscle tumors that were commonly categorized as GISTs in the past. GISTs are typically c-Kit–positive, whereas leiomyomas are desmin-positive and c-Kit–negative.54 The sizes can vary greatly, ranging from less than 0.5 cm to 20 cm. Both GISTs and leiomyomas can grow inwardly and outwardly to form a dumbbell shape, although leiomyomas are more likely to grow intraluminally (vs GISTs, which expand predominantly in an extramural fashion).90

These lesions are typically asymptomatic and found incidentally.91-93 Endoscopically, they appear as rounded submucosal lesions with intact overlying mucosa.90 When palpated, they feel “rubbery.” The histologic distinction between well-differentiated leiomyosarcoma and leiomyomas can be difficult with EUS fine-needle aspiration or true-cut biopsy and the minimum diagnostic criteria for leiomyosarcomas are poorly defined.94-96 In a retrospective analysis of 53 EUS cases (7 leiomyomas and 46 GISTs), EUS features, such as inhomogeneity, hyperechoic foci, and a marginal halo, help to differentiate GISTs from leiomyomas.54

Granular Cell Tumors

Although commonly found in the esophagus, rare cases of granular cell tumors originating in the stomach have been reported.97 They tend to occur equally in both sexes, commonly in the fourth to sixth decade of life.98 For unknown reasons, about half of granular cell tumors occur synchronously with esophageal granular cell tumors.98 They occur in the proximal stomach and range from a few millimeters in size up to 7 cm. Endoscopically, they are usually found incidentally and appear as yellow subepithelial masses or nodules, often mistaken for lipomas, although firmer on biopsy.98 Histologically, the tumors arise in the submucosa. Most are benign, but reports of malignancy exist.99


In summary, gastric polyps are a common finding during routine endoscopy. Despite the fact that more than 90% are asymptomatic and do not have malignant potential, a subset of gastric polyps require further intervention, and histologic evaluation is necessary to determine the type of polyp and the presence of dysplasia. The identification of such polyps requires histologic evaluation and may involve additional diagnostic investigative techniques, such as tandem biopsies, immunohistochemistry staining, endoscopic ultrasound, and endoscopic ultrasound-assisted tissue acquisition. Furthermore, it is essential for gastroenterologists to provide full endoscopic and clinical information to the pathologist to reach a proper diagnosis since many conditions have similar histologic characteristics.


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